These data indicate that HSV-1 UL12.5 deploys cellular proteins, including ENDOG and EXOG, to destroy mtDNA and contribute to a growing body of literature highlighting roles for ENDOG and EXOG in mtDNA maintenance.

Conclude that EndoG and TOPO2a may actively participate in apoptotic chromatin degradation.

Mouse (Murine) Endonuclease G (ENDOG) interaction partners

These results support the involvement of redox signaling in the control of cardiomyocyte growth by ENDOG and suggest a pathway relating mtDNA content to the regulation of cell growth probably involving humanin, which prevents reactive oxygen radicals accumulation and hypertrophy induced by Endog deficiency.

Deficiency of AKT2 in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG, which is also regulated by AKT2, is a suppressor of MEF2A in myocardium.

increased browning of white adipose tissue elicited by the lack of EndoG was associated with a better glucose tolerance and reduced fat mass

This study demonistated that Endonuclease G knockout mice reveals a new putative molecular player in the regulation of anxiety.

These findings determine a role for EndoG in the generation of Switch region double-strand DNA breaks and class switch DNA recombination.

EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation

endonuclease G is essential for embryonic survival, but not through a mitochondrial or apoptosis function

These data suggest that the early nuclear translocation of endoG occurs and could induce DNA fragmentation in the ischemic brain after cerebral ischemia.

EndoG null mice are viable and develop to adulthood with no obvious abnormalities, suggesing that EndoG is not essential for early embryogenesis and apoptosis.

Overexpression of DNase I in cultured mouse tubular epithelial cells also induced EndoG. Both DNase I and EndoG mediate cisplatin injury to tubular epithelial cells.

high levels of EndoG were found in adult liver, heart, muscle & to a lesser extent, brain & kidney; EndoG had little or no expression in adult spleen & in embryonic organs at E13.5 stage

The translocation of EndoG to the nucleus of neurons in the infarct implicates EndoG in ischemic neuronal degeneration after permanent MCA occlusion in mice.

Mouse EndoG without the mitochondrial localization signal (amino-acid residues 1-43) was successfully overexpressed, purified and crystallized using a microbatch method under oil

Data demonstrate the importance of DNase I and EndoG in host cell defense against gene and RNA delivery to renal tubular epithelial cells in vitro.

Endo G has a role in neuronal cell death as a result of oxidative stress.

Cow (Bovine) Endonuclease G (ENDOG) interaction partners

Results describe the mechanism of catalysis and substrate binding by the apoptotic mitochondrial nuclease EndoG, which belongs to the large family of DNA/RNA non-specific betabetaalpha-Me-finger nucleases.

Endonuclease G (ENDOG) profil antigène

Antigen Summary

The protein encoded by this gene is a nuclear encoded endonuclease that is localized in the mitochondrion. The encoded protein is widely distributed among animals and cleaves DNA at GC tracts. This protein is capable of generating the RNA primers required by DNA polymerase gamma to initiate replication of mitochondrial DNA.